Dr. Karl E. Klose’s Laboratory

Stephen Rodriguez

Stephen Rodriguez, Graduate Student
Tel.: 210-458-7033
e-mail: Stephen.Rodriguez@utsa.edu
e-mail: lqd555@my.utsa.edu

Tularemia is a zoonotic disease caused by the bacterium Francisella tularensis.  F. tularensis can cause high morbidity and mortality when acquired through the pulmonary route; thus, the CDC has categorized this bacterium as a category A select agent and a potential biological weapon. A cluster of virulence genes, the Francisella Pathogenicity Island (FPI), has been identified as directly involved in intramacrophage survival and growth of F. tularensis. Thus, characterization of the FPI genes is a prime focus of our research in F. tularensis.
Different subspecies of F. tularensis demonstrate different levels of virulence in humans. One of the chromosomal characteristics that distinguishes the high virulence (for humans) subspecies tularensis from the low virulence (for humans) novicida subspecies is the presence of two identical copies of the FPI in the high virulence subspecies.  My research has focused on developing novel genetic techniques to inactivate duplicated FPI genes within the high virulence subspecies.  This led to the development of a technique utilizing Group II introns (targetron) that efficiently inactivates duplicated FPI genes in a single step. My current work is concentrated on determining the effect of FPI copy number on F. tularensis virulence, as well as characterizing individual FPI proteins for their function and contribution to intramacrophage survival and growth.

Targetron plasmid:  plasmid pKEK1140 was constructed to adapt the Targetron system for disruption of F. tularensis genes.  Critical components for adaptation were the following:  group II intron (LtrB), intron encoded protein (LtrA), F. tularensis ori, antibiotic resistance cassette, F. tularensis promoters.

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South Texas Center for Emerging Infectious Diseases
Department of Biology
University of Texas at San Antonio